Rev Fac Cien Med Univ Nac Cordoba
December 2024
As Drumond Rennie put it, ‘Science does not come alive until it is shared publicly’ (1998), emphasising that the rapid advancement of scientific research requires its efficient and rigorous dissemination both to encourage the development of new strategies and to avoid duplication of effort and resources. The current model of scientific and technological research is facing a significant challenge: the cost associated with publishing its results. It is now increasingly common for publishers to impose fees on the scientific community to publish their results, generating debate about the impact of this practice on the fairness of scientific dissemination.
View Article and Find Full Text PDFIntroduction: Coronavirus disease 2019 (COVID-19) affects the population unequally, with a greater impact on older and immunosuppressed people.
Methods: Hence, we performed a prospective experimental cohort study to characterise the effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination in immune-compromised patients (older adults and oncohaematologic patients), compared with healthy counterparts, based on deep characterisation of the circulating immune cell subsets.
Results And Discussion: While acquired humoral and cellular memory did not predict subsequent infection 18 months after full vaccination, spectral and computational cytometry revealed several subsets within the CD8 T-cells, B-cells, natural killer (NK) cells, monocytes and TEMRA Tγδ cells that were differentially expressed in individuals who were subsequently infected and not infected not just following immunisation, but also prior to vaccination.
Chronic kidney disease (CKD) is a growing health concern, projected to be a major cause of death by 2040, due to an increasing risk of acute kidney injury (AKI). Systems biology-derived data suggest that the unmet need for an orally available drug to treat AKI and improve CKD outcomes may be addressed by targeting kidney inflammation and, specifically, nuclear factor κB-inducing kinase (NIK), a key signaling molecule that activates the noncanonical nuclear factor κB (NF-κB) pathway. We have prepared and identified a small family of imidazolone derivatives that bind NIK and inhibit the noncanonical NF-κB activation pathway.
View Article and Find Full Text PDFSeveral data indicate that Substance P (SP) neurokinin type 1 receptor (NK1R) is at the center of the interaction between cancer cells and peripheral sensory neurons. Selecting the appropriate cancer cell line and its susceptibility to being modulated by NK1 antagonists are critical to studying this complex interaction. In the current study, we have focused on this selection by comparing several aspects of the triple-negative breast cancer (TNBC) cell line (MDA-MB-231) with a modified murine cell line (E0771), both expressing luciferase.
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